It is known that humans exhibit circadian cycles in a variety of physiologic, cognitive, and behavioral functions. The cycles are driven by an internal biological clock or circadian pacemaker which is located in the brain. It is also known that humans exhibit different degrees of alertness or productivity during different phases of their circadian cycle.
Often, the activities in which humans wish to engage do not coincide with the most appropriate point in their circadian cycle. For instance, transmeridian travelers experience what is commonly referred to as "jet lag", due to the fact that their circadian cycle is not "in tune" with the geophysical time of their destination. In essence, the traveler's physiological cycle either lags or leads their desired activity-rest schedule.
In a similar fashion, people who work in professions requiring them to work at night, such as factory workers, medical personnel, and police experience a desynchrony between the activities in which they desire to engage and their physiological ability to engage in such activities. Commonly known as "shift workers" these individuals often experience an inability to sleep soundly during their non-working hours.
Other sleep-related disorders thought to be related to the misalignment of the circadian cycle with the desired activity-rest schedule include delayed-sleep-phase insomnia, advanced-sleep-phased insomnia and Seasonal Affective Disorder (SAD).
It has been known for quite some time that the circadian cycle of all animals (including humans) is sensitive to exposure to bright light. Thus, it is recognized that the circadian cycle of an animal may be adjusted or modified by exposing the subject to scheduled "pulses" of bright light.
Although all animals are responsive to applications of bright light, the responsiveness of the circadian pacemaker of all animals is not the same. For example, the responsiveness of the circadian pacemaker of a rodent is quite different than the responsiveness of the circadian pacemaker of a human. Indeed, for over twenty years it has been recognized that the response of the circadian pacemaker to light in nocturnal rodents is principally developed during the early time of light exposure (e.g., within the first 15 minutes from the dark-adapted state) while subsequent protracted exposure (e.g., 1-2 hours) generates relatively little additional phase shift. Recently, these findings were considerably sharpened for the case of the golden hamster. See Nelson, D. E. et al., "Sensitivity and Integration in a Visual Pathway for Circadian Entrainment in the Hamster (Mesocricetus Auratus),"Journal of Physiology, No. 439 (1991), pp. 115-145. A tradeoff between light intensity and stimulus duration was demonstrated (i.e., brighter light requires less duration), and at a modest level of light (e.g., 20 lux) pseudo-saturation of the phase shift response was achieved in about five minutes.
Superficially, the responsiveness of the human circadian pacemaker to light is very different. Unquestionably, humans are less sensitive, requiring several thousand lux of light and stimulus durations of several hours to match rodent phase shifts achieved at 20 lux of light in 5 minutes. This is consistent, however, with the high sensitivity of nocturnal rodents for all visual tasks. It was recently discovered that a significant functional distinction between rodents and humans is the fact that humans appear to sum circadian photic responses progressively. For example, three hours of exposure to bright light produces about 3/5 the phase shift of five hours of exposure to light centered at the same point of the circadian phase.
The apparently disparate functional characteristics of human and rodent responses can actually be described as a manifestation of a single model structure which is the subject of the present invention.